Exposure to air pollution impairs cellular energy metabolism

Date:
June 15, 2020
Source:
University of Eastern Finland
Summary:
Exposure to air particulate matter impairs the metabolism of
olfactory mucosal cells, according to a recent study. The results
can contribute to a better understanding of how air pollutants
may harm brain health, as the olfactory mucosa can act as a key
pathway to the brain.



FULL STORY ========================================================================== Exposure to air particulate matter impairs the metabolism of olfactory
mucosal cells, according to a recent study from the University of Eastern Finland. The results can contribute to a better understanding of how
air pollutants may harm brain health, as the olfactory mucosa can act
as a key pathway to the brain.


==========================================================================
In the last decade, the adverse effects of ambient air pollutants,
including particulate matter, on the central nervous system is
increasingly reported by epidemiological, animal and post-mortem
studies. Exposure to air pollutants has been associated with
neurodegenerative disorders, among other things. The association of
air pollutant exposure with deteriorating brain health is speculated
to be driven by particulate matter entry via the olfactory mucosa,
a neural tissue located at the upper part of the nasal cavity. The
olfactory mucosa consists of a mixture of diverse cell types that are
important for the sense of smell, as the only neural tissue outside of
the brain. It acts as a first line of defence against inhaled agents,
including air pollutants. How air pollutant exposure affects this key
brain entry site remains elusive.

The original research article published in Particle and Fibre Toxicology
by the research group of Associate Professor Katja Kanninen from the
University of Eastern Finland, sheds light on how exposure to particulate matter impacts the function of the human olfactory mucosa. The study was carried out with a new cellular model based on primary human olfactory
mucosal cells.

Using sophisticated functional measurements and transcriptomic analyses,
the researchers found that particulate matter exposure causes critical impairment in the metabolism of olfactory mucosal cells. These
functions of mitochondria, the cellular organelles responsible for
energy production, are disturbed by air pollutants. The researchers also identified the mitochondria-targeted NPTX1 gene, which has been shown previously to be associated with brain disorders, as a key driver of mitochondrial dysfunction upon particulate matter exposure.

According to Associate Professor Kanninen, the research carried out at
the University of Eastern Finland may provide important insight into
the effects of harmful environmental agents on the brain.

"Given the importance of the nasal cavity as a potential gateway to the
brain by particles and external invaders, I believe that more studies
should focus on discovering how exposure to environmental agents and
factors affects the olfactory mucosa. This may one day lead to new ways
of limiting the adverse health effects of airborne particle exposure," Associate Professor Kanninen notes.


========================================================================== Story Source: Materials provided by University_of_Eastern_Finland. Note: Content may be edited for style and length.


========================================================================== Journal Reference:
1. Sweelin Chew, Riikka Lampinen, Liudmila Saveleva, Paula Korhonen,
Nikita
Mikhailov, Alexandra Grubman, Jose M. Polo, Trevor Wilson, Mika
Komppula, Teemu Ro"nkko", Cheng Gu, Alan Mackay-Sim, Tarja Malm,
Anthony R. White, Pasi Jalava, Katja M. Kanninen. Urban air
particulate matter induces mitochondrial dysfunction in human
olfactory mucosal cells. Particle and Fibre Toxicology, 2020; 17
(1) DOI: 10.1186/s12989-020-00352-4 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2020/06/200615100929.htm

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